a cure for cancer case study quizlet

• Patient Care & Health Information
• Diseases & Conditions

Cancer screening

Diagnosing cancer at its earliest stages often provides the best chance for a cure. With this in mind, talk with your doctor about what types of cancer screening may be appropriate for you.

For a few cancers, studies show that screening tests can save lives by diagnosing cancer early. For other cancers, screening tests are recommended only for people with increased risk.

A variety of medical organizations and patient-advocacy groups have recommendations and guidelines for cancer screening. Review the various guidelines with your doctor and together you can determine what's best for you based on your own risk factors for cancer.

Cancer diagnosis

Your doctor may use one or more approaches to diagnose cancer:

• Physical exam. Your doctor may feel areas of your body for lumps that may indicate cancer. During a physical exam, your doctor may look for abnormalities, such as changes in skin color or enlargement of an organ, that may indicate the presence of cancer.
• Laboratory tests. Laboratory tests, such as urine and blood tests, may help your doctor identify abnormalities that can be caused by cancer. For instance, in people with leukemia, a common blood test called complete blood count may reveal an unusual number or type of white blood cells.
• Imaging tests. Imaging tests allow your doctor to examine your bones and internal organs in a noninvasive way. Imaging tests used in diagnosing cancer may include a computerized tomography (CT) scan, bone scan, magnetic resonance imaging (MRI), positron emission tomography (PET) scan, ultrasound and X-ray, among others.

Biopsy. During a biopsy, your doctor collects a sample of cells for testing in the laboratory. There are several ways of collecting a sample. Which biopsy procedure is right for you depends on your type of cancer and its location. In most situations, a biopsy is the only way to definitively diagnose cancer.

In the laboratory, doctors look at cell samples under the microscope. Normal cells look uniform, with similar sizes and orderly organization. Cancer cells look less orderly, with varying sizes and without apparent organization.

Cancer stages

Once cancer is diagnosed, your doctor will work to determine the extent (stage) of your cancer. Your doctor uses your cancer's stage to determine your treatment options and your chances for a cure.

Staging tests and procedures may include imaging tests, such as bone scans or X-rays, to see if cancer has spread to other parts of the body.

Cancer stages are indicated by the numbers 0 through 4, which are often written as Roman numerals 0 through IV. Higher numbers indicate a more-advanced cancer. For some types of cancer, cancer stage is indicated using letters or words.

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Cancer care at Mayo Clinic

• Biopsy procedures
• Cancer blood tests
• Cancer survival rate
• Atypical cells: Are they cancer?
• Small cell, large cell cancer: What this means
• Tumor vs. cyst: What's the difference?
• Complete blood count (CBC)
• Needle biopsy

Many cancer treatments are available. Your treatment options will depend on several factors, such as the type and stage of your cancer, your general health, and your preferences. Together you and your doctor can weigh the benefits and risks of each cancer treatment to determine which is best for you.

Cancer Clinical Trials Offer Many Benefits

Goals of cancer treatment.

Cancer treatments have different objectives, such as:

• Cure. The goal of treatment is to achieve a cure for your cancer, allowing you to live a normal life span. This may or may not be possible, depending on your specific situation.

Primary treatment. The goal of a primary treatment is to completely remove the cancer from your body or kill the cancer cells.

Any cancer treatment can be used as a primary treatment, but the most common primary cancer treatment for the most common cancers is surgery. If your cancer is particularly sensitive to radiation therapy or chemotherapy, you may receive one of those therapies as your primary treatment.

Adjuvant treatment. The goal of adjuvant therapy is to kill any cancer cells that may remain after primary treatment in order to reduce the chance that the cancer will recur.

Any cancer treatment can be used as an adjuvant therapy. Common adjuvant therapies include chemotherapy, radiation therapy and hormone therapy.

Palliative treatment. Palliative treatments may help relieve side effects of treatment or signs and symptoms caused by cancer itself. Surgery, radiation, chemotherapy and hormone therapy can all be used to relieve symptoms and control the spread of cancer when a cure isn't possible. Medications may relieve symptoms such as pain and shortness of breath.

Palliative treatment can be used at the same time as other treatments intended to cure your cancer.

Cancer treatments

Doctors have many tools when it comes to treating cancer. Cancer treatment options include:

• Surgery. The goal of surgery is to remove the cancer or as much of the cancer as possible.
• Chemotherapy. Chemotherapy uses drugs to kill cancer cells.
• Radiation therapy. Radiation therapy uses high-powered energy beams, such as X-rays and protons, to kill cancer cells. Radiation treatment can come from a machine outside your body (external beam radiation), or it can be placed inside your body (brachytherapy).

Bone marrow transplant. Bone marrow transplant is also known as a stem cell transplant. Your bone marrow is the material inside your bones that makes blood cells. A bone marrow transplant can use your own cells or cells from a donor.

A bone marrow transplant allows your doctor to use higher doses of chemotherapy to treat your cancer. It may also be used to replace diseased bone marrow.

• Immunotherapy. Immunotherapy, also known as biological therapy, uses your body's immune system to fight cancer. Cancer can survive unchecked in your body because your immune system doesn't recognize it as an intruder. Immunotherapy can help your immune system "see" the cancer and attack it.
• Hormone therapy. Some types of cancer are fueled by your body's hormones. Examples include breast cancer and prostate cancer. Removing those hormones from the body or blocking their effects may cause the cancer cells to stop growing.
• Targeted drug therapy. Targeted drug treatment focuses on specific abnormalities within cancer cells that allow them to survive.
• Clinical trials. Clinical trials are studies to investigate new ways of treating cancer. Thousands of cancer clinical trials are underway.

Other treatments may be available to you, depending on your type of cancer.

• Adjuvant therapy for cancer
• Cancer pain: Relief is possible
• Cancer surgery
• Cancer treatment myths
• Cancer-related diarrhea
• Cancer-related fatigue
• Eating during cancer treatment: Tips to make food tastier
• Low blood counts
• Monoclonal antibody drugs
• Mouth sores caused by cancer treatment: How to cope
• No appetite? How to get nutrition during cancer treatment
• Chemotherapy side effects: A cause of heart disease?
• Biological therapy for cancer
• Bone marrow transplant
• Cancer treatment
• Chemotherapy
• Intensity-modulated radiation therapy (IMRT)
• Palliative care
• Radiation therapy
• PICC line placement
• Infographic: Cancer Clinical Trials Offer Many Benefits

Clinical trials

Explore Mayo Clinic studies testing new treatments, interventions and tests as a means to prevent, detect, treat or manage this condition.

Alternative medicine

No alternative cancer treatments have been proved to cure cancer. But alternative medicine options may help you cope with side effects of cancer and cancer treatment, such as fatigue, nausea and pain.

Talk with your doctor about which alternative medicine options may offer some benefit. Your doctor can also discuss whether these therapies are safe for you or whether they may interfere with your cancer treatment.

Some alternative medicine options found to be helpful for people with cancer include:

• Acupuncture
• Relaxation techniques
• Curcumin: Can it slow cancer growth?
• High-dose vitamin C: Can it kill cancer cells?

Coping and support

A cancer diagnosis can change your life forever. Each person finds his or her own way of coping with the emotional and physical changes cancer brings. But when you're first diagnosed with cancer, sometimes it's difficult to know what to do next.

Here are some ideas to help you cope:

• Learn enough about cancer to make decisions about your care. Ask your doctor about your cancer, including your treatment options and, if you like, your prognosis. As you learn more about cancer, you may become more confident in making treatment decisions.
• Keep friends and family close. Keeping your close relationships strong will help you deal with your cancer. Friends and family can provide the practical support you'll need, such as helping take care of your house if you're in the hospital. And they can serve as emotional support when you feel overwhelmed by cancer.

Find someone to talk with. Find a good listener who is willing to listen to you talk about your hopes and fears. This may be a friend or family member. The concern and understanding of a counselor, medical social worker, clergy member or cancer support group also may be helpful.

Ask your doctor about support groups in your area. Other sources of information include the National Cancer Institute and the American Cancer Society.

Preparing for your appointment

Start by making an appointment with your doctor if you have any signs or symptoms that worry you. If your doctor determines that you have cancer, you'll likely be referred to one or more specialists, such as:

• Doctors who treat cancer (oncologists)
• Doctors who treat cancer with radiation (radiation oncologists)
• Doctors who treat diseases of the blood and blood-forming tissues (hematologists)

Because appointments can be brief, and because there's often a lot information to discuss, it's a good idea to be prepared. Here's some information to help you get ready, and know what to expect from your doctor.

What you can do

• Be aware of any pre-appointment restrictions. At the time you make the appointment, be sure to ask if there's anything you need to do in advance, such as restrict your diet.
• Write down any symptoms you're experiencing, including any that may seem unrelated to the reason for which you scheduled the appointment.
• Write down key personal information, including any major stresses or recent life changes.
• Write down your family's history of cancer. If other members of your family have been diagnosed with cancer, make a note of the types of cancer, how each person is related to you and how old each person was when diagnosed.
• Make a list of all medications, vitamins or supplements that you're taking.
• Consider taking a family member or friend along. Sometimes it can be difficult to remember all the information provided during an appointment. Someone who accompanies you may remember something that you missed or forgot.
• Write down questions to ask your doctor.

Your time with your doctor is limited, so preparing a list of questions can help you make the most of your time together. List your questions from most important to least important in case time runs out. For cancer, some basic questions to ask your doctor include:

• What type of cancer do I have?
• What stage is my cancer?
• Will I need additional tests?
• What are my treatment options?
• Can treatments cure my cancer?
• If my cancer can't be cured, what can I expect from treatment?
• What are the potential side effects of each treatment?
• Is there one treatment you feel is best for me?
• How soon do I need to begin treatment?
• How will treatment affect my daily life?
• Can I continue working during treatment?
• Are there any clinical trials or experimental treatments available to me?
• I have these other health conditions. How can I manage them during my cancer treatment?
• Are there any restrictions that I need to follow?
• Should I see a specialist? What will that cost, and will my insurance cover it?
• Is there a generic alternative to the medicine you're prescribing?
• Are there brochures or other printed material that I can take with me? What websites do you recommend?
• What will determine whether I should plan for follow-up visits?

In addition to the questions that you've prepared to ask your doctor, don't hesitate to ask other questions that occur to you.

What to expect from your doctor

Your doctor is likely to ask you a number of questions. Being ready to answer them may allow time later to cover other points you want to address. Your doctor may ask:

• When did you first begin experiencing symptoms?
• Have your symptoms been continuous or occasional?
• How severe are your symptoms?
• What, if anything, seems to improve your symptoms?
• What, if anything, appears to worsen your symptoms?
• Does anyone in your family have cancer?
• Have you ever had cancer before? If so, what kind and how was it treated?
• Have you ever been exposed to chemicals at home or at work?
• Do you smoke or use tobacco?
• Have you ever been diagnosed with a hepatitis infection or a human papillomavirus infection?
• Cancer. World Health Organization. https://www.who.int/news-room/fact-sheets/detail/cancer. Accessed Feb. 16, 2021.
• Cancer stat facts: Cancer of any site. National Cancer Institute Surveillance, Epidemiology, and End Results Program. https://seer.cancer.gov/statfacts/html/all.html. Accessed Feb. 16, 2021.
• Symptoms of cancer. National Cancer Institute. https://www.cancer.gov/about-cancer/diagnosis-staging/symptoms. Accessed Feb. 16, 2021.
• Rock CL, et al. American Cancer Society guideline for diet and physical activity for cancer prevention. CA: A Cancer Journal for Clinicians. 2020;doi:doi.org/10.3322/caac.21591.
• Niederhuber JE, et al., eds. Genetic and epigenetic alterations in cancer. In: Abeloff's Clinical Oncology. 6th ed. Elsevier; 2020. https://www.clinicalkey.com. Accessed Dec. 4, 2020.
• Ulcerative colitis. National Institute of Diabetes and Digestive and Kidney Diseases. https://www.niddk.nih.gov/health-information/digestive-diseases/ulcerative-colitis/all-content. Accessed Feb. 16, 2021.
• Paraneoplastic syndromes information page. National Institute of Neurological Disorder and Stroke. https://www.ninds.nih.gov/Disorders/All-Disorders/Paraneoplastic-Syndromes-Information-Page. Accessed Feb. 16, 2021.
• Deng GE, et al. Evidence-based clinical practice guidelines for integrative oncology: Complementary therapies and botanicals. Journal of the Society for Integrative Oncology. 2009;7:85.
• Taking time: Support for people with cancer. National Cancer Institute. https://www.cancer.gov/publications/patient-education/taking-time. Accessed Feb. 16, 2021.
• The American Cancer Society, eds. The principles and drivers of cancer. In: The American Cancer Society's Principles of Oncology: Prevention to Survivorship. Wiley-Blackwell; 2018.
• Hypercalcemia (high level of calcium in the blood). Merck Manual Consumer Edition. https://www.merckmanuals.com/home/hormonal-and-metabolic-disorders/electrolyte-balance/hypercalcemia-high-level-of-calcium-in-the-blood#. Accessed Feb. 16, 2021.
• What is cancer? National Cancer Institute. https://www.cancer.gov/about-cancer/understanding/what-is-cancer. Accessed Feb. 16, 2021.
• Cancer prevention overview (PDQ) — Health professional version. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/hp-prevention-overview-pdq. Accessed Feb. 16, 2021.
• The genetics of cancer. National Cancer Institute. https://www.cancer.gov/about-cancer/causes-prevention/genetics. Accessed Feb. 16, 2021.
• Understanding cancer risk. Cancer.Net. https://www.cancer.net/navigating-cancer-care/prevention-and-healthy-living/understanding-cancer-risk. Accessed Feb. 16. 2021.
• Cancer screening overview (PDQ) — Health professional version. National Cancer Institute. https://www.cancer.gov/about-cancer/screening/hp-screening-overview-pdq. Accessed Feb. 16, 2021.
• How cancer is diagnosed. National Cancer Institute. https://www.cancer.gov/about-cancer/diagnosis-staging/diagnosis. Accessed Feb. 16, 2021.
• Cancer staging. National Cancer Institute. https://www.cancer.gov/about-cancer/diagnosis-staging/staging. Accessed Feb. 16, 2021.
• Making decisions about cancer treatment. Cancer.Net. https://www.cancer.net/navigating-cancer-care/how-cancer-treated/making-decisions-about-cancer-treatment. Accessed Feb. 16, 2021.
• How cancer is treated. Cancer.Net. https://www.cancer.net/navigating-cancer-care/how-cancer-treated. Accessed Feb. 16, 2021.
• Absolute risk
• Cancer diagnosis: 11 tips for coping
• Cancer risk: What the numbers mean
• Cancer survivors: Care for your body after treatment
• Cancer survivors: Late effects of cancer treatment
• Cancer survivors: Managing your emotions after cancer treatment
• Heart cancer: Is there such a thing?
• How cancer spreads
• Image-guided needle biopsy
• Mort Crim and Cancer
• Myths about cancer causes
• Punch biopsy
• Relative risk
• Self-Image During Cancer
• What does cancer look like?
• When cancer returns: How to cope with cancer recurrence

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Cancer Drugs Practice Questions with Answers and NCLEX ® Review

Cancer is one of the most difficult diseases to manage. Cancer can affect more than one body system at a time. Therefore, nurses need to have basic knowledge of pharmacokinetics (absorption, distribution, metabolism, and excretion) of chemotherapy to provide adequate client care.

Cancer Drugs Practice Questions with Answers

Learning outcomes, test taking tips, introduction to cancer drugs.

Cancer is a disease caused when cells divide uncontrollably and spread into surrounding tissues. Changes to DNA cause cancer. Cancerous cells can form a mass of tissue known as a tumor. Before the cancer is even detectable, the cells can break off of the tumor and spread to other parts of the body, where they begin to grow and multiply. This process is called metastasis .

Treatment regimens can be quite challenging related to many factors such as age, weight, diagnosis, prognosis, and even the client’s health before the diagnosis. There are many chemotherapy, biotherapy, and immunotherapy medications that can be prescribed.

Chemotherapy drugs are designed to help slow or stop the growth of cancer cells. They work by damaging DNA in cancer cells and killing them. However, it does not differentiate between good and bad cells. In other words, chemotherapy can kill good cells also. Chemotherapy targets rapidly dividing cells, creating the majority of side effects experienced with the medication.

Immunotherapy (Biotherapy)

A newer type of treatment for cancer is immunotherapy (a type of biotherapy), which signals the immune system to fight off cancer cells. One such drug is Interferon .

Interferons are substances produced by cells in the body to help fight infections and tumors. It’s typically used to treat melanoma but can also treat other cancers such as leukemia and AIDS-related Kaposi’s sarcoma. Interferon can also be used to treat hepatitis B and C.

Chemotherapy Drugs

Chemotherapy drugs work by damaging or killing rapidly-dividing cells, such as those in cancers and infections – genetic material in cells, which prevents them from reproducing. They suppress the immune system and destroy rapidly dividing cells, including cancer cells.

Chemotherapy drugs can be given by multiple routes such as, topically, intravenously, intramuscular, intracavitary, and subcutaneously. A few of the most common chemotherapy drugs are Doxorubicin , Cisplatin , and Cyclophosphamide .

Indication: Slow and stop the growth of tumors.

Mechanism of action: Directly inhibiting growing cells in the body.

Side effects ( that result from the rapidly dividing cells):

• Loss of appetite

Interferon is a protein that’s produced by cells in response to viral infection. It’s used for treating several types of cancer, including melanoma and breast cancer, but it also has some side effects. Interferon is administered through injection or intravenous infusion into the vein or muscle. Several different regimens are used for this type of medication.

The most common side effects are flu-like symptoms. These usually go away within a few days of starting treatment and don’t last long after clients stop taking interferon:

• Sore throat

Interferon has been used as a cancer treatment for decades, but it’s not a cure. When interferon is injected into the body, it can act as an antiviral agent and stop the growth of cancer cells.

During my exam, I could literally see and hear him going over different areas as I was answering my questions.

This past Friday I retook my Maternity Hesi and this time, I decided for my last week of Holiday break to just watch all of his OB videos. I am proud to say that with Mike’s help I received a score of 928 on my Maternity Hesi!

Cancer Drugs Conclusion

Creating a treatment plan can be challenging for clients with cancer, especially when considering medications. 

For clients on a regimen of chemotherapy, there is much to consider, and it’s challenging to treat cancer clients. These medications kill rapidly dividing cells and not just cancer cells. This can result in many side effects, including low blood cell counts (which will also result in immunosuppression). 

Although immunotherapy has some negative effects, it can effectively treat several cancers. There are promising results that immunotherapy and biotherapy may be able to completely eradicate all cancerous cells within a tumor without harming the healthy tissue around it.  There are also hopes that it does not result in unpleasant side effects associated with conventional chemotherapy.

https://www.ncbi.nlm.nih.gov/books/NBK564367  

https://www.cancer.org/treatment/treatments-and-side-effects/treatment-types/chemotherapy/how-chemotherapy-drugs-work.html  

https://www.cancer.org/treatment/treatments-and-side-effects/treatment-types/immunotherapy/what-is-immunotherapy.html  

https://www.cancerresearchuk.org/about-cancer/cancer-in-general/treatment/cancer-drugs/drugs/interferon

https://www.mayoclinic.org/tests-procedures/chemotherapy/about/pac-20385033

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In Search of a Cure for Breast Cancer

By Jolanta Skalska

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In this directed case study, students analyze data, draw a research-based conclusion, interpret experimental results, and discuss the relevance of research findings for clinical practice. Specifically, students examine the effects of chemotherapeutic drugs on newly generated cell lines and explain research outcomes using their prior knowledge of signal transduction pathways (G-protein coupled receptors), hormones, glycolysis, oxidative phosphorylation, and DNA structure and function as they follow the story of "Emily," an undergraduate student who is accepted into an internship program focusing on the breast cancer cell line MCF-7. Emily learns that MCF-7 cells can survive the treatment of tamoxifen and a hormone deprivation regimen, which leads to the generation of new cell lines (Tam3 and TamR3) that do not activate the mTOR signaling pathway. Emily attempts to predict how the Tam3 and TamR3 cells will respond to the mTOR inhibitor rapamycin, and then incorporates drugs used for chemotherapy into her experiments. Originally written for upper-level undergraduate biology majors, the case study is also appropriate for courses focusing on cell biology, pharmacology, and cancer biology.

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Date Posted

• List the functions of the steroid hormones, classify receptors, and summarize the mechanism of action and effects of chemotherapeutic drugs.
• Interpret experimental data and explain the outcomes of experiments described in the case study.
• Determine the differences between cell lines based on data, present signaling transduction pathways, and predict research outcomes.
• Explain the phenotypical differences between three cell lines, debate experimental outcomes and present them in the form of a written discussion.

Breast cancer; camptothecin; competitive inhibitor; cisplatin; doxorubicin; fluorouracil; G-protein coupled receptors; MCF-7; ER+; PR+; membrane receptors; mTOR; signaling pathway; oxidative phosphorylation; reactive oxygen species; tamoxifen

Subject Headings

EDUCATIONAL LEVEL

Undergraduate upper division

TOPICAL AREAS

TYPE/METHODS

Teaching Notes & Answer Key

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Teaching notes are intended to help teachers select and adopt a case. They typically include a summary of the case, teaching objectives, information about the intended audience, details about how the case may be taught, and a list of references and resources.

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Materials & Media

Supplemental materials.

The optional PowerPoint presentation below can be used to pace students as they work through the case study in class.

• breast_cancer_direct.pptx (~100 KB)

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Stem Cell Transplants in Cancer Treatment

To collect stem cells for a stem cell transplant, the donor is connected to an apheresis machine. After the machine collects blood stem cells from the donor, it returns the rest of the blood to their body.

Stem cell  transplants are procedures that restore blood stem cells in people who have had theirs destroyed by the high doses of chemotherapy or radiation therapy that are used to treat certain cancers, blood disorders, and autoimmune disorders. Blood-forming stem cells are vital because they grow into different types of blood cells. The main types of blood cells are:

• white blood cells, which are part of your immune system and help your body fight infection
• red blood cells, which carry oxygen throughout your body
• platelets, which help the blood clot and prevent bleeding

Types of cancer treated with stem cell transplants

Stem cell transplants are most often used to treat people with cancers that affect blood cells, such as leukemia , lymphoma , multiple myeloma , and myelodysplastic syndromes . They may also be used for  neuroblastoma , Ewing sarcoma ,  brain tumors that have come back in children, germ cell tumors , and testicular cancer . 

Stem cell transplants are also used for other blood disorders, such as aplastic anemia , sickle cell disease , and autoimmune diseases.

Stem cell transplants for other types of cancer are being studied in clinical trials, which are research studies involving people. To find a study that may be an option for you, see  Find a Clinical Trial .

How stem cell transplants work against cancer

Stem cell transplants do not usually work against cancer directly. Instead, they restore your body's ability to produce new blood cells after treatment with the very high doses of chemotherapy and maybe other treatments, such as radiation therapy, that are used to destroy cancer cells.

But in leukemia, the stem cell transplant may work against cancer directly. This happens because of an effect called graft-versus-tumor or graft-versus-leukemia, which can occur after transplants that use stem cells from a donor. This effect occurs when white blood cells from your donor (the graft) attack any cancer cells that remain in your body (the tumor or leukemia cells). This effect improves the chances of success of the transplant.

Types of stem cell transplants

In a stem cell transplant, you receive healthy blood-forming stem cells through a needle in your vein. Most of the blood-forming stem cells that are used in transplants come from the bloodstream. When stem cells come from the blood, the transplant may be called a peripheral blood stem cell transplant , or PBSCT. But blood stem cells can also come from the bone marrow or umbilical cord, which is blood collected when a baby is born. When the stem cells come from the bone marrow, the procedure may be called a bone marrow transplant , or BMT. When they come from cord blood, the procedure may be called a cord blood transplant. 

Once they enter your bloodstream, the stem cells travel to the bone marrow, where they take the place of the cells that were destroyed by treatment. Transplants can be:

• autologous, which means the stem cells come from you, the person with cancer
• allogeneic, which means the stem cells come from someone else. The donor may be a blood relative or someone who is not related, if the cells are a close enough match to yours
• syngeneic, which means the stem cells come from your identical twin

There are benefits and risks to both autologous and allogeneic stem cell transplants. With autologous transplants, the transplanted cells will match. But there is a small risk that cancer cells will be transplanted. 

With allogeneic transplants, it is important that the cells match closely enough that your immune system won’t see the transplanted blood stem cells as foreign and destroy them.

Mini-transplants are a type of allogeneic transplant that use lower doses of cancer treatment than a regular transplant. They do not kill all your blood-forming stem cells, but they still kill some of the cancer cells. This type of allogeneic transplant can prevent rejection of the donor’s stem cells by suppressing your immune system.

Tandem transplants are a type of autologous transplant. During a tandem transplant, you receive a round of high-dose chemotherapy followed by a stem cell transplant. Then after many weeks or months, you have another round of high-dose chemotherapy followed by another stem cell transplant. 

Whether a stem cell transplant is right for you and which type you might have depends on many factors, such as:

• the type of cancer you have
• how advanced your cancer is
• if you can use your own stem cells
• if matching donor stem cells are available
• if there are other treatments that are likely to work for your cancer
• if you can tolerate high doses of chemotherapy
• if you have other serious health problems
• other treatments you’ve had in the past

Your doctor will carefully weigh these issues with the risks and benefits of each type of stem cell transplant and discuss them with you.

How blood-forming stem cells are matched

To decide if the stem cells from a donor are a match for you, they will be tested for their HLAs (which stands for human leukocyte antigens ). HLAs are sets of proteins , or markers, that you have on most cells in your body. Each person has a different set of HLAs. The more HLAs that you and the donor have in common, the better the chance that your body will accept the donor’s stem cells.

Most often, the best match for an allogeneic stem cell transplant is a brother or sister.

See Donating Blood Stem Cells for Stem Cell Transplants to learn about stem cell donation.

Stem cell transplant side effects

The high doses of cancer treatment that you have before a stem cell transplant can cause problems such as: 

Side Effects of Cancer Treatment

Learn how to manage or treat side effects caused by cancer or cancer treatments.

• increased risk of infection
• feeling tired and exhausted

Stem cell transplants may cause both short- and long-term problems. Short-term problems may include:

• loss of appetite
• mouth sores
• skin reactions 

Long-term problems of stem cell transplants may include:

• infertility
• cataracts (clouding of the lens of the eye, which causes loss of vision)
• new secondary cancers
• liver, kidney, lung, or heart damage
• bone and muscle weakness 

Talk with your doctor or nurse about side effects that you might have, how serious they might be, and what to do about them. 

Tell your doctor or nurse if you have trouble eating during stem cell transplant. You might find it helpful to speak with a  dietitian . 

For more information about side effects and how to manage them, see  Side Effects of Cancer Treatment.

Graft-versus-host disease (GVHD)

If you have an allogeneic transplant, you might develop a serious problem called graft-versus-host disease . Graft-versus-host disease can occur when white blood cells from your donor (the graft) see cells in your body (the host) as foreign and attack them. This problem can cause damage to your skin, liver, intestines, and many other organs. 

Graft-versus-host disease can be acute or chronic. Acute graft-versus-host disease occurs within the first 3 months after transplant. Chronic graft-versus-host disease occurs 3 months after a transplant or later.

Graft-versus-host disease can be treated with steroids or other drugs that suppress your immune system .

There are a few ways that the risk of graft-versus-host disease can be reduced.

• The closer your donor’s stem cells match yours, the less likely you are to have graft-versus-host disease. 
• Your doctor may give you drugs to suppress your immune system.
• Donated stem cells can be treated to remove the white blood cells (called T cells ) that cause graft-versus-host disease. This process is called T-cell depletion .

How much stem cell transplants cost

Stem cells transplants are complicated procedures that are very expensive. They require long hospital stays at special treatment centers and require the services of many health care providers. If you do not live nearby, you will need to stay in a hotel or apartment when you are not in the hospital. If you have no problems, you can go home 100 days after you’ve received the donor stem cells. But you will need to be closely followed by a doctor who has experience in taking care of people who have had a stem cell transplant.

Transplants can cause serious side effects that can be expensive to manage. 

If you need to travel for treatment, you might have extra costs for transportation, housing, and childcare.  

Most insurance plans cover some of the costs of transplants for certain types of cancer. Talk with your health plan about which services it will pay for. The business office of your treatment center may help you understand all the costs involved. 

To learn about groups that may be able to provide financial help, go to the National Cancer Institute database,  Organizations that Offer Support Services , and search "financial assistance." Or contact NCI’s Cancer Information Service for information about groups that may be able to help.

Where you go for a stem cell transplant

When you need an allogeneic stem cell transplant, you will need to go to a hospital that has a specialized transplant center. The National Marrow Donor Program® maintains a  list of transplant centers in the United States .

How long it takes to have a stem cell transplant

A stem cell transplant can take a few months to complete. The process begins with treatment with high doses of chemotherapy and maybe radiation therapy. This treatment goes on for a week or two. Once you have finished, you will have a few days to rest.

Next, you will receive the blood stem cells. The day you receive your stem cells is often called “day zero.” The stem cells will be given to you through an intravenous (IV) catheter. This process is like receiving a blood transfusion . It takes 1 to 5 hours to receive all the stem cells. 

After receiving the stem cells, you begin the recovery phase. During this time, doctors will follow the progress of the new blood cells by checking your blood counts often. As the new stem cells produce blood cells, your blood counts will go up.

Even after your blood counts return to normal, it takes much longer for your immune system to fully recover—several months for autologous transplants, and 1 to 2 years for allogeneic or syngeneic transplants.

How you may feel after a stem cell transplant

Stem cell transplants affect people in different ways. How you feel depends on:

• the type of transplant that you have
• the doses of treatment you have before the transplant
• how you respond to the high-dose treatments
• your type of cancer
• how healthy you were before the transplant

Since people respond to stem cell transplants in different ways, your doctor or nurses cannot know for sure how the procedure will make you feel.

Working during a stem cell transplant

Going Back to Work

Information and guidance on going back to work, including talking with and relating to others at work, your legal rights, and handling problems at work.

Whether or not you can work during a stem cell transplant may depend on the type of job you have. The process of a stem cell transplant, with the high-dose treatments, the transplant, and recovery, can take many months. You will be in and out of the hospital during this time. Even when you are not in the hospital, sometimes you will need to stay near it, rather than staying in your own home. 

You will be more tired and your ability to concentrate on work may be affected. You will be visiting the hospital two or three times a week after discharge. You may need to spend a few hours in the hospital for blood or platelet transfusions or replacing minerals in your body.

So, if your job allows, you may want to arrange to work remotely part-time. Many employers are required by law to change your work schedule to meet your needs during cancer treatment. Talk with your employer about ways to adjust your work during treatment. You can learn more about these laws by talking with a social worker.

For more information about working with cancer and your legal rights, see Going Back to Work .

Stem cell transplants in clinical trials

If you are interested in finding a stem cell transplant clinical trial, use the advanced clinical trials search form or contact NCI's Cancer Information Service .

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Nutrition and cancer: A review of the evidence for an anti-cancer diet

Michael s donaldson.

1 Director of Research, Hallelujah Acres Foundation, 13553 Vantage Hwy, Ellensburg, WA 98926, USA

It has been estimated that 30–40 percent of all cancers can be prevented by lifestyle and dietary measures alone. Obesity, nutrient sparse foods such as concentrated sugars and refined flour products that contribute to impaired glucose metabolism (which leads to diabetes), low fiber intake, consumption of red meat, and imbalance of omega 3 and omega 6 fats all contribute to excess cancer risk. Intake of flax seed, especially its lignan fraction, and abundant portions of fruits and vegetables will lower cancer risk. Allium and cruciferous vegetables are especially beneficial, with broccoli sprouts being the densest source of sulforophane. Protective elements in a cancer prevention diet include selenium, folic acid, vitamin B-12, vitamin D, chlorophyll, and antioxidants such as the carotenoids (α-carotene, β-carotene, lycopene, lutein, cryptoxanthin). Ascorbic acid has limited benefits orally, but could be very beneficial intravenously. Supplementary use of oral digestive enzymes and probiotics also has merit as anticancer dietary measures. When a diet is compiled according to the guidelines here it is likely that there would be at least a 60–70 percent decrease in breast, colorectal, and prostate cancers, and even a 40–50 percent decrease in lung cancer, along with similar reductions in cancers at other sites. Such a diet would be conducive to preventing cancer and would favor recovery from cancer as well.

The field of investigation of the role of nutrition in the cancer process is very broad. It is becoming clearer as research continues that nutrition plays a major role in cancer. It has been estimated by the American Institute for Cancer Research and the World Cancer Research Fund that 30–40 percent of all cancers can be prevented by appropriate diets, physical activity, and maintenance of appropriate body weight [ 1 ]. It is likely to be higher than this for some individual cancers.

Most of the research on nutrition and cancer has been reductionist; that is, a particular food or a nutrient has been studied in relation to its impact on tumor formation/regression or some other end point of cancer at a particular site in the body. These studies are very helpful in seeing the details of the mechanisms of disease. However, they do not help give an overall picture of how to prevent cancer on a dietary level. Even less, they tell little of how to eat when a person already has a cancer and would like to eat a diet that is favorable to their recovery.

This review will focus on those dietary factors which has been shown to be contribute to increased risk of cancer and then on those additional protective dietary factors which reduce cancer risk. Finally, some whole-diet studies will be mentioned which give a more complete picture of how these individual factors work together to reduce cancer risk.

Over Consumption of Energy (Calories)

Eating too much food is one of the main risk factors for cancer. This can be shown two ways: (1) by the additional risks of malignancies caused by obesity, and (2) by the protective effect of eating less food.

Obesity has reached epidemic proportions in the United States. Sixty-four percent of the adult population is overweight or obese [ 2 ]. About 1 in 50 are now severely obese (BMI > 40 kg/m2) [ 3 ]. Mokdad et al [ 4 ] found that poor diet and physical inactivity was the second leading cause of death (400,000 per year in the USA), and would likely overtake tobacco as the leading cause of death.

It was estimated in a recent study, from a prospective cancer prevention cohort, that overweight and obesity accounted for 14 percent of all cancer deaths in men and 20 percent of those in women [ 5 ]. Significant positive associations were found between obesity and higher death rates for the following cancers: esophagus, colon and rectum, liver, gallbladder, pancreas, kidney, stomach (in men), prostate, breast, uterus, cervix, and ovary [ 5 ]. The authors estimated that over 90,000 cancer deaths per year could be avoided if the adult population all maintained a normal weight (BMI < 25.0) [ 5 ]. Clearly, obesity is a major risk factor for cancer.

On the other side, careful menu planning brings about an approach entitled CRON-Calorie Restriction with Optimal Nutrition. The basic idea is to eat a reduced amount of food (about 70–80 percent of the amount required to maintain "normal" body weight) while still consuming all of the necessary amounts of vitamins, minerals, and other necessary nutrients. The only restriction is the total amount of energy (calories) that is consumed. While being difficult to practice, this approach has a lot of scientific merit for being able to extend average life spans of many species of animals including rats, mice, fish, and possibly primates (currently being tested). Along with this life span extension is a reduction in chronic diseases that are common to mankind, reviewed in Hursting et al [ 6 ]. A recent meta-analysis of 14 experimental studies found that energy restriction resulted in a 55% reduction in spontaneous tumors in laboratory mice [ 7 ]. Calorie restriction inhibited induced mammary tumors in mice [ 8 ] and suppressed implanted tumor growth and prolonged survival in energy restricted mice [ 9 ]. Among Swedish women who had been hospitalized for anorexia nervosa (definitely lower caloric intake, but not adequate nutrition) prior to age 40, there was a 23% lower incidence of breast cancer for nulliparous women and a 76% lower incidence for parous women [ 10 ]. So, too many calories is definitely counter-productive, and slightly less than normal is very advantageous.

Glucose Metabolism

Refined sugar is a high energy, low nutrient food – junk food. "Unrefined" sugar (honey, evaporated cane juice, etc) is also very concentrated and is likely to contribute to the same problems as refined sugar. Refined wheat flour products are lacking the wheat germ and bran, so they have 78 percent less fiber, an average of 74 percent less of the B vitamins and vitamin E, and 69 percent less of the minerals (USDA Food database, data not shown). Concentrated sugars and refined flour products make up a large portion of the carbohydrate intake in the average American diet. One way to measure the impact of these foods on the body is through the glycemic index.

The glycemic index is an indication of the blood sugar response of the body to a standardized amount of carbohydrate in a food. The glycemic load takes into account the amount of food eaten. An international table of the glycemic index and glycemic load of a wide variety of foods has been published [ 11 ].

Case-control studies and prospective population studies have tested the hypothesis that there is an association between a diet with a high glycemic load and cancer. The case control studies have found consistent increased risk of a high glycemic load with gastric [ 12 ], upper aero digestive tract [ 13 ], endometrial [ 14 ], ovarian [ 15 ], colon or colorectal cancers [ 16 , 17 ]. The prospective studies' results have been mixed. Some studies showed increased risk of cancer in the whole cohort with high glycemic load [ 18 - 20 ]; some studies found only increased risk among subgroups such as sedentary, overweight subjects [ 21 - 24 ]; other studies concluded that there was no increased risk for any of their cohort [ 25 - 28 ]. Even though there were no associations between glycemic load and colorectal, breast, or pancreatic cancer in the Nurses' Health Study there was still a strong link between diabetes and colorectal cancer [ 29 ].

Perhaps the dietary glycemic load is not consistently related to glucose disposal and insulin metabolism due to individual's different responses to the same glycemic load. Glycated hemoglobin (HbA 1c ) is a time-integrated measurement of glucose control, and indirectly, of insulin levels. Increased risk in colorectal cancer was seen in the EPIC-Norfolk study with increasing HbA 1c ; subjects with known diabetes had a three-fold increased risk of colorectal cancer [ 30 ]. In a study of a cohort in Washington county, Maryland, increased risk of colorectal cancer was seen in subjects with elevated HbA 1c , BMI > 30 kg/m 2 , or who used medications to control diabetes [ 31 ]. However, glycated hemoglobin was not found to be associated with increased risk of colorectal cancer in a small nested case-control study within the Nurses' Health Study [ 32 ]. Elevated fasting glucose, fasting insulin, 2 hour levels of glucose and insulin after an oral glucose challenge, and larger waist circumference were associated with a higher risk of colorectal cancer [ 33 ]. In multiple studies diabetes has been linked with increased risk of colorectal cancer [ 34 - 37 ], endometrial cancer [ 38 ], and pancreatic cancer [ 35 , 39 ]. It is clear that severe dysregulation of glucose metabolism is a risk factor for cancer. Foods which contribute to hyperinsulinemia, such as refined sugar, foods containing refined sugar, and refined flour products should be avoided and eliminated from a cancer protective diet.

Unrefined plant foods typically have an abundance of fiber. Dairy products, eggs, and meat all have this in common – they contain no fiber. Refined grain products also have most of the dietary fiber removed from them. So, a diet high in animal products and refined grains (a typical diet in the USA) is low in fiber. In prospective health studies low fiber was not found to be a risk for breast cancer [ 25 ]. It is possible that fiber measurements are just a surrogate measure for unrefined plant food intake. Slattery et al [ 40 ] found an inverse correlation between vegetable, fruit and whole grain intake plant food intake and rectal cancer, while refined grains were associated with increased risk of rectal cancer. A threshold of about 5 daily servings of vegetables was needed to reduce cancer risk and the effect was stronger among older subjects [ 40 ]. Many other nutrients are co-variants with fiber, including folic acid, which is covered in detail below.

Red meat has been implicated in colon and rectal cancer. A Medline search in February 2003 uncovered 26 reports of human studies investigating the link between diet and colon or colorectal cancer. Of the 26 reports, 21 of them reported a significant positive relationship between red meat and colon or colorectal cancer [ 17 , 41 - 64 ]. A recent meta-analysis also found red meat, and processed meat, to be significantly associated with colorectal cancer [ 65 ]. Meat, and the heterocyclic amines formed in cooking, have been correlated to breast cancer in a case-control study in Uruguay as well [ 66 ].

Omega 3:6 Ratio Imbalance

Omega 3 fats (alpha-linolenic acid, EPA, DHA) have been shown in animal studies to be protect from cancer, while omega 6 fats (linoleic acid, arachidonic acid) have been found to be cancer promoting fats. Now there have been several studies that have tested this hypothesis in relation to breast cancer, summarized in Table ​ Table1. 1 . Except for the study by London et al [ 67 ], all of these studies found an association between a higher ratio of N-3 to N-6 fats and reduced risk of breast cancer. Long chain N-3 and N-6 fats have a different effect on the breast tumor suppressor genes BRCA1 and BRCA2. Treatment of breast cell cultures with N-3 fats (EPA or DHA) results in increased expression of these genes while arachadonic acid had no effect [ 68 ]. Flax seed oil and DHA (from an algae source) both can be used to increase the intake of N-3 fat, with DHA being a more efficient, sure source.

Breast Cancer and Omega 3:6 Ratio.

Flax seed provides all of the nutrients from this small brown or golden hard-coated seed. It is an excellent source of dietary fiber, omega 3 fat (as alpha-linolenic acid), and lignans. The lignans in flax seed are metabolized in the digestive tract to enterodiol and enterolactone, which have estrogenic activity. In fact, flax seed is a more potent source of phytoestrogens than soy products, as flax seed intake caused a bigger change in the excretion of 2-hydroxyestrone compared to soy protein [ 69 ].

Ground flax seeds have been studied for its effect on cancer, including several excellent studies by Lilian Thompson's research group at the University of Toronto. In one study the flax seed, its lignan fraction, or the oil were added to the diet of mice who had previously been administered a chemical carcinogen to induce cancer. All three treatments reduced the established tumor load; the lignan fraction containing secoisolariciresinol diglycoside (SDG) and the flax seed also reduced metastasis [ 70 ]. In another study the flax lignan SDG was fed to mice starting 1 week after treatment with the carcinogen dimethylbenzanthracene. The number of tumors per rat was reduced by 46% compared to the control in this study [ 71 ]. Flax or its lignan (SDG) were tested to see if they would prevent melanoma metastasis. The flax or lignan fraction were fed to mice two weeks before and after injection of melanoma cells. The flax treatment (at 2.5, 5, or 10% of diet intake) resulted in a 32, 54, and 63 percent reduction in the number of tumors, compared to the control [ 72 ]. The SDG, fed at amounts equivalent to the amount in 2.5, 5, or 10% flax seed, also reduced the tumor number, from a median number of 62 in the control group to 38, 36, and 29 tumors per mouse in the SDG groups, respectively [ 73 ].

More recently Thompson's research group studied mice that were injected with human breast cancer cells. After the injection the mice were fed a basal diet (lab mouse chow) for 8 weeks while the tumors grew. Then one group continued the basal diet and another was fed a 10% flax seed diet. The flax seed reduced the tumor growth rate and reduced metastasis by 45% [ 74 ].

Flax seed has been shown to enhance mammary gland morphogenesis or differentiation in mice. Nursing dams were fed the 10% flax seed diet (or an equivalent amount of SDG). After weaning the offspring mice were fed a regular mouse chow diet. Researchers then examined the female offspring and found an increased number of terminal end buds and terminal ducts in their mammary glands with more epithelial cell proliferation, all demonstrating that mammary gland differentiation was enhanced [ 75 ]. When these female offspring were challenged with a carcinogen to induce mammary gland tumors there were significantly lower incidence of tumors (31% and 42% lower in the flax seed and SDG groups, respectively), significantly lower tumor load (51% and 62% lower in the flax seed and SDG groups, respectively), significantly lower mean tumor size (44% and 68% lower in the flax seed and SDG groups, respectively), and significantly lower tumor number (47% and 45% lower in the flax seed and SDG groups, respectively) [ 76 ]. So, flax seed and its lignan were able to reduce tumor growth (both in number and size of tumors), prevent metastasis, and even cause increased differentiation of mouse mammary tissue in suckling mice, making the offspring less susceptible to carcinogenesis even when not consuming any flax products.

Other researchers have tested flax seed and prostate cancer. In an animal model using mice, Lin et al [ 77 ] found that a diet supplemented with 5% flax inhibited the growth and development of prostate cancer in their experimental mouse model. A pilot study of 25 men who were scheduled for prostatectomy surgery were instructed to eat a low-fat diet (20% or less of energy intake) and to supplement with 30 g of ground flaxseed per day. During the follow-up of an average of 34 days there were significant changes in serum cholesterol, total testosterone, and the free androgen index [ 78 ]. The mean proliferation index of the experimental group was significantly lower and apoptotic indexes higher compared to historical matched controls. Ground flax seed may be a very beneficial food for men battling prostate cancer. However, a meta-analysis of nine cohort and case-control studies revealed an association between flax seed oil intake or high blood levels of alpha-linolenic acid and prostate cancer risk [ 79 ]. It is quite likely that the lignans in flax seed are a major component of flax's anti-cancer effects so that flax oil without the lignans is not very beneficial. Some brands of flax seed oil retain some of the seed particulate because of the beneficial properties of the lignans.

Fruits and Vegetables

One of the most important messages of modern nutrition research is that a diet rich in fruits and vegetables protects against cancer. (The greatest message is that this same diet protects against almost all other diseases, too, including cardiovascular disease and diabetes.) There are many mechanisms by which fruits and vegetables are protective, and an enormous body of research supports the recommendation for people to eat more fruits and vegetables.

Block et al [ 80 ] reviewed about 200 studies of cancer and fruit and vegetable intake. A statistically significant protective effect of fruits and vegetables was found in 128 of 156 studies that gave relative risks. For most cancers, people in the lower quartile (1/4 of the population) who ate the least amount of fruits and vegetables had about twice the risk of cancer compared to those who in the upper quartile who ate the most fruits and vegetables. Even in lung cancer, after accounting for smoking, increasing fruits and vegetables reduces lung cancer; an additional 20 to 33 percent reduction in lung cancers is estimated [ 1 ].

Steinmetz and Potter reviewed the relationship between fruits, vegetables, and cancer in 206 human epidemiologic studies and 22 animal studies [ 81 ]. They found "the evidence for a protective effect of greater vegetable and fruit consumption is consistent for cancers of the stomach, esophagus, lung, oral cavity and pharynx, endometrium, pancreas, and colon." Vegetables, and particularly raw vegetables, were found to be protective; 85% of the studies that queried raw vegetable consumption found a protective effect. Allium vegetables, carrots, green vegetables, cruciferous vegetables, and tomatoes also had a fairly consistent protective effect [ 81 ]. Allium vegetables (garlic, onion, leeks, and scallions) are particularly potent and have separately been found to be protective for stomach and colorectal cancers [ 82 , 83 ] and prostate cancer [ 84 ].

There are many substances that are protective in fruits and vegetables, so that the entire effect is not very likely to be due to any single nutrient or phytochemical. Steinmetz and Potter list possible protective elements: dithiolthiones, isothiocyanates, indole-32-carbinol, allium compounds, isoflavones, protease inhibitors, saponins, phytosterols, inositol hexaphosphate, vitamin C, D-limonene, lutein, folic acid, beta carotene (and other carotenoids), lycopene, selenium, vitamin E, flavonoids, and dietary fiber [ 81 ].

A joint report by the World Cancer Research Fund and the American Institute for Cancer Research found convincing evidence that a high fruit and vegetable diet would reduce cancers of the mouth and pharynx, esophagus, lung, stomach, and colon and rectum; evidence of probable risk reduction was found for cancers of the larynx, pancreas, breast, and bladder [ 1 ].

Many of the recent reports from prospective population-based studies of diet and cancer have not found the same protective effects of fruits and vegetables that were reported earlier in the epidemiological and case-control studies [reviewed in [ 85 ]]. One explanation is that people's memory of what they ate in a case-cohort study may have been tainted by their disease state. Another problem might be that the food frequency questionnaires (FFQ) used to measure food intake might not be accurate enough to detect differences. Such a problem was noted in the EPIC study at the Norfolk, UK site. Using a food diary the researchers found a significant correlation between saturated fat intake and breast cancer, but using a FFQ there was no significant correlation [ 86 ]. So, inaccurate measurement of fruit and vegetable intake might be part of the explanation as well.

It must be noted that upper intakes of fruits and vegetables in these studies are usually within the range of what people on an American omnivorous diet normally eat. In the Nurses Health Study the upper quintiles of fruit and vegetable intake were 4.5 and 6.2 servings/day, respectively [ 87 ]. Similarly, the upper quintiles of fruit and vegetable intake in the Health Professionals Follow-up Study were 4.3 and 5.4 serving/day for fruits and vegetables, respectively [ 87 ]. Intakes of fruits and vegetables on the Hallelujah Diet are much higher, with median reported intakes of six servings of fruits (646 g/day) and eleven servings of vegetables per day (971 g/day) [ 88 ] in addition to a green powder from the juice of barley leaves and alfalfa that is equivalent to approximately another 100 g/day of fresh dark greens. So, it is very possible that the range of intakes in the prospective population based studies do not have a wide enough intake on the upper end to detect the true possible impact of a very high intake of fruits and vegetables on cancer risk.

Cruciferous Vegetables

Cruciferous vegetables (broccoli, cauliflower, cabbage, Brussels sprouts) contain sulforophane, which has anti-cancer properties. A case-control study in China found that intake of cruciferous vegetables, measured by urinary secretion of isothiocyanates, was inversely related to the risk of breast cancer; the quartile with the highest intake only had 50% of the risk of the lowest intake group [ 89 ]. In the Nurses' Health Study a high intake of cruciferous vegetables (5 or more servings/week vs less than two servings/week) was associated with a 33% lower risk of non-Hodgkin's lymphoma [ 90 ]. In the Health Professionals Follow-up Study bladder cancer was only weakly associated with low intake of fruits and vegetables, but high intake (5 or more servings/week vs 1 or less servings/wk) of cruciferous vegetables was associated with a statistically significant 51% decrease in bladder cancer [ 91 ]. Also, prostate cancer risk was found to be reduced by cruciferous vegetable consumption in a population-based case-control study carried out in western Washington state. Three or more servings per week, compared to less than one serving of cruciferous vegetables per week resulted in a statistically significant 41% decrease in prostate cancer risk [ 92 ]. Similar protective effects of cruciferous vegetables were seen in a multi-ethnic case-control study [ 93 ]. A prospective study in Shanghai, China found that men with detectable amounts of isothiocyanates in their urine (metabolic products that come from cruciferous vegetables) had a 35% decreased risk of lung cancer. Among men that had one or two genetic polymorphisms that caused them to eliminate these isothiocyanates slower there was a 64% or 72% decreased risk of lung cancer, respectively [ 94 ].

Broccoli sprouts have a very high concentration of sulforophane since this compound originates in the seed and is not made in the plant as it grows [ 95 , 96 ]. One sprout contains all of the sulforophane that is present in a full-grown broccoli plant. So, if sulforophane is especially cancer-protective, it would seem reasonable to include some broccoli sprouts in an anti-cancer diet.

Selenium is a mineral with anti-cancer properties. Many studies in the last several years have shown that selenium is a potent protective nutrient for some forms of cancer. The Arizona Cancer Center posted a selenium fact sheet listing the major functions of selenium in the body [ 97 ]. These functions are as follows:

1. Selenium is present in the active site of many enzymes, including thioredoxin reductase, which catalyze oxidation-reduction reactions. These reactions may encourage cancerous cells to under apoptosis.

2. Selenium is a component of the antioxidant enzyme glutathione peroxidase.

3. Selenium improved the immune systems' ability to respond to infections.

4. Selenium causes the formation of natural killer cells.

5. P450 enzymes in the liver may be induced by selenium, leading to detoxification of some carcinogenic molecules.

6. Selenium inhibits prostaglandins that cause inflammation.

7. Selenium enhances male fertility by increased sperm motility.

8. Selenium can decrease the rate of tumor growth.

A serendipitous randomized, double-blind, controlled trial of a 200 μg/day selenium supplement in the southeastern region of the USA (where soil selenium levels are low) found that the primary endpoints of skin cancer were not improved by the selenium supplement, but that other cancer incidence rates were decreased by selenium [ 98 , 99 ]. There was a significant reduction in total cancer incidence (105 vs 137 cases, P = 0.03), prostate cancer (22 vs 42 cases, P = 0.005), a marginally significant reduction in colorectal cancer incidence (9 vs 19 cases, P = 0.057), and a reduction in cancer mortality, all cancer sites (40 vs 66 deaths, P = 0.008) (selenium versus control group cases reported, respectively) [ 98 ]. The selenium supplement was most effective in ex-smokers and for those who began the study with the lowest levels of serum selenium. Several prospective studies have also examined the role of selenium in cancer prevention, particularly for prostate cancer, summarized in Table ​ Table2 2 .

Prospective Nested Case Control Studies of Selenium and Prostate Cancer.

Overall, it appears that poor selenium levels, especially for men, are a cancer risk. If a person has low selenium levels and other antioxidant defenses are also low the cancer risk is increased even further. Women do not appear to be as sensitive to selenium, as breast cancer has not been found to be influenced by selenium status in several studies [ 100 - 104 ], although both men and women were found to be protected by higher levels of selenium from colon cancer [ 100 ] and lung cancer [ 105 , 106 ]. Good vegetarian sources of selenium are whole grains and legumes grown in selenium-rich soil in the western United States, brazil nuts (by far the most dense source of selenium), nutritional yeast, brewers yeast, and sunflower seeds.

Chlorophyll

All green plants also contain chlorophyll, the light-collecting molecule. Chlorophyll and its derivatives are very effective at binding polycyclic aromatic hydrocarbons (carcinogens largely from incomplete combustion of fuels), heterocyclic amines (generated when grilling foods), aflatoxin (a toxin from molds in foods which causes liver cancer), and other hydrophobic molecules. The chlorophyll-carcinogen complex is much harder for the body to absorb, so most of it is swept out with the feces. The chemoprotective effect of chlorophyll and its derivatives has been tested in laboratory cell cultures and animals [ 107 , 108 ]. There is so much compelling evidence for anti-carcinogenic effects of chlorophyll that a prospective randomized controlled trial is being conducted in Qidong, China to see if chlorophyllin can reduce the amount of liver cancer cases, which arise from aflatoxin exposure in their foods (corn, peanuts, soy sauce, and fermented soy beans). A 55% reduction in aflatoxin-DNA adducts were found in the group that took 100 mg of chlorophyllin three times a day [ 109 ]. It was supposed that the chlorophyllin bound up aflatoxins, but there were chlorophyllin derivatives also detected in the sera (which had a green tint to it) of the volunteers who took the supplement, indicating a possible role in the body besides binding carcinogens in the gut [ 110 ].

Protective Vitamins

Vitamin b-12.

Vitamin B-12 has not been proven to be an anti-cancer agent, but there is some evidence indicating that it could be beneficial. The form of administered vitamin B-12 may be important.

Some experimental cancer studies have been carried out with various forms of vitamin B-12. Methylcobalamin inhibited tumor growth of SC-3 injected into mice [ 111 ], and caused SC-3 mouse mammary tumor cells to undergo apoptosis, even when stimulated to grow by the presence of growth-inducing androgen [ 112 ]. Methylcobalamin, but not cyanocobalamin, increased the survival time of mice bearing implanted leukemia tumor cells [ 113 ]. 5'-deoxyadenosylcobalamin and methylcobalamin, but not cyanocobalamin, were shown to be effective cytotoxic agents [ 114 ]. Methylcobalamin also was able to increase survival time and reduce tumor growth in laboratory mice [ 115 ].

Laboratory mechanistic evidence for the effects of vitamin B12 were seen in a laboratory study with vitamin B-12 deficient rats. Choi et al [ 116 ] found that the colonic DNA of the B-12 deficient rats had a 35% decrease in genomic methylation and a 105% increase in uracil incorporation, both changes that could increase risk of carcinogenesis. In two prospective studies (one in Washington Country, Maryland and the Nurses' Health Study) a relation between lower vitamin B12 status (but not deficiency) and statistically significant higher risk of breast cancer was found [ 117 , 118 ]. So, there is evidence from laboratory studies, prospective cohort studies, and mechanistic studies showing that vitamin B-12 is an important nutrient for genetic stability, DNA repair, carcinogenesis, and cancer therapy.

Folic acid is the dark green leafy vegetable vitamin. It has an integral role in DNA methylation and DNA synthesis. Folic acid works in conjunction with vitamin B-6 and vitamin B-12 in the single carbon methyl cycle. If insufficient folic acid is not available uracil is substituted for thymidine in DNA, which leads to DNA strand breakage. About 10% of the US population (and higher percentages among the poor) has low enough intakes of folic acid to make this a common problem [ 119 ]. As shown in Tables ​ Tables3 3 and ​ and4, 4 , many studies have found a significant reduction in colon, rectal, and breast cancer with higher intakes of folic acid and their related nutrients (vitamin B-6 and B-12). Alcohol is an antagonist of folate, so that drinking alcoholic beverages greatly magnifies the cancer risk of a low-folate diet. Genetic polymorphisms (common single DNA base mutations resulting in a different amino acid encoded into a protein) in the methylenetetrahydrofolate reductase and the methionine synthase genes which increase the relative amount of folate available for DNA synthesis and repair also reduces the risk of colon cancer [ 120 - 123 ]. Cravo et al [ 124 ] used 5 mg of folic acid a day (a supraphysiological dose) in a prospective, controlled, cross-over study of 20 patients with colonic adenoma polyps. They found that the folic acid could reverse DNA hypomethylation in 7 of 12 patients who had only one polyp.

Folate and Colon / Rectal Cancer.

SS = statistically significant

Prospective Studies of Folate and Breast Cancer.

FH = Family History

Folate may be more important for rapidly dividing tissue, like the colonic mucosa. Therefore, the cancer risk associated with low folate intake is probably higher for colon cancer than for breast cancer. Most of the breast cancer studies only found a protective effect of folate among women who consumed alcohol (see Table ​ Table4). 4 ). However, among women residents of Shanghai who consumed no alcohol, no vitamin supplements and ate unprocessed, unfortified foods there was a 29% decreased risk of breast cancer among those with the highest intake of folate [ 125 ]. So, there may be a true protective effect that is masked in the western populations by so many other risk factors. Two studies showed that the risk of cancer due to family history can be modified by high folate intake, so a prudent anti-cancer diet would be high in dark green leafy vegetables. The mean intake of folic acid on the Hallelujah Diet was 594 μg/day for men and 487 μg/day for women [ 88 ].

Vitamin D is produced primarily from the exposure of the skin to sunshine. Even casual exposure of the face, hands, and arms in the summer generates a large amount of vitamin D. In fact, simulated sunshine, equivalent to standing on a sunny beach until a slight pinkness of the skin was detected, was equivalent to a 20,000 IU oral dose of vitamin D 2 [ 126 ]. (Note that the RDA is 400 IU for most adults.) It has been estimated that 1,000 IU per day is the minimal amount needed to maintain adequate levels of vitamin D in the absence of sunshine [ 126 ], and that up to 4,000 IU per day can be safely used with additional benefit [ 127 ].

The concentration of the active hormonal form of vitamin D is tightly regulated in the blood by the kidneys. This active hormonal form of vitamin D has the potent anti-cancer properties. It has been discovered that various types of normal and cancerous tissues, including prostate cells [ 128 ], colon tissue [ 129 ], breast, ovarian and cervical tissue [ 130 ], pancreatic tissue [ 131 ] and a lung cancer cell line [ 132 ] all have the ability to convert the major circulating form of vitamin D, 25(OH)D, into the active hormonal form, 1,25(OH) 2 D. So, there is a local mechanism in many tissues of the body for converting the form of vitamin D in the body that is elevated by sunshine exposure into a hormone that has anticancer activity.

Indeed, 25(OH)D has been shown to inhibit growth of colonic epithelial cells [ 133 ], primary prostatic epithelial cells [ 134 ], and pancreatic cells [ 131 ]. So, the laboratory work is confirming what had been seen some time ago in ecological studies of populations and sunshine exposure.

The mortality rates for colon, breast, and ovary cancer in the USA show a marked north-south gradient [ 135 ]. In ecological studies of populations and sunlight exposure (no individual data) sunlight has been found to have a protective effect for prostate cancer [ 136 ], ovarian cancer [ 137 ], and breast cancer [ 138 ]. Recently Grant found that sunlight was also protective for bladder, endometrial, renal cancer, multiple myeloma, and Non-Hodgkins lymphoma in Europe [ 139 ] and bladder, esophageal, kidney, lung, pancreatic, rectal, stomach, and corpus uteri cancer in the USA [ 140 ]. Several prospective studies of vitamin D and cancer have also shown a protective effect of vitamin D (see Table ​ Table5). 5 ). It could be that sunshine and vitamin D are protective factors for cancers of many organs that can convert 25(OH)D into 1,25(OH)D 2 .

Prospective Studies of Vitamin D and Cancer.

Antioxidants

α- and β-carotene and other carotenoids.

Carotenoids have been studied vigorously to see if these colorful compounds can decrease cancer risk. In ecological studies and early case-control studies it appeared that β-carotene was a cancer-protective agent. Randomized controlled trials of β-carotene found that the isolated nutrient was either neutral [ 141 ] or actually increased risk of lung cancer in smokers [ 142 , 143 ]. Beta-carotene may be a marker for intake of fruits and vegetables, but it does not have a powerful protective effect in isolated pharmacological doses.

However, there is a large body of literature that indicates that dietary carotenoids are cancer preventative (See Table ​ Table6). 6 ). Alpha-carotene has been found to be a stronger protective agent than its well-known isomer β-carotene. Studies tend to agree that overall intake of carotenoids is more protective than a high intake of a single carotenoid. So, a variety of fruits and vegetables is still a better anti-cancer strategy than just using a single vegetable high in a specific carotenoid.

Studies of Carotenoids and Lung Cancer.

SS = statistically significant difference between comparison groups.

The richest source of α-carotene is carrots and carrot juice, with pumpkins and winter squash as a second most-dense source. There is approximately one μg of α-carotene for every two μg of β-carotene in carrots. The most common sources of β-cryptoxanthin are citrus fruits and red sweet peppers.

Of the various carotenoids lycopene has been found to be very protective, particularly for prostate cancer. The major dietary source of lycopene is tomatoes, with the lycopene in cooked tomatoes being more bioavailable than that in raw tomatoes. Several prospective cohort studies have found associations between high intake of lycopene and reduced incidence of prostate cancer, though not all studies have produced consistent results [ 144 , 145 ]. Some studies suffer from a lack of good correlation between lycopene intake assessed by questionnaire and actual serum levels, and other studies measured intakes among a population that consumed very few tomato products. The studies with positive results will be reviewed here.

In the Health Professionals Follow-up Study there was a 21% decrease in prostate cancer risk, comparing the highest quintile of lycopene intake with the lowest quintile. Combined intake of tomatoes, tomato sauce, tomato juice, and pizza (which accounted for 82% of the lycopene intake) were associated with a 35% lower risk of prostate cancer. Furthermore, lycopene was even more protective for advanced stages of prostate cancer, with a 53% decrease in risk [ 146 ]. A more recent follow-up report on this same cohort of men confirmed these original findings that lycopene or frequent tomato intake is associated with about a 30–40% decrease in risk of prostate cancer, especially advanced prostate cancer [ 147 ].

In addition to the two reports above a nested case control study from the Health Professional Follow-up Study with 450 cases and controls found an inverse relation between plasma lycopene and prostate cancer risk (OR 0.48) among older subjects (>65 years of age) without a family history of prostate cancer [ 148 ]. Among younger men high plasma β-carotene was associated with a statistically significant 64% decrease in prostate cancer risk. So, the results for lycopene have been found for dietary intakes as well as plasma levels.

In a nested case-control study from the Physicians' Health Study cohort, a placebo-controlled study of aspirin and β-carotene, there was a 60% reduction in advanced prostate cancer risk (P-trend = 0.006) for those subjects in the placebo group with the highest plasma lycopene levels, compared to the lowest quintile. The β-carotene also had a protective effect, especially for those men with low lycopene levels [ 149 ].

In addition to these observational studies, two clinical trials have been conducted to supplement lycopene for a short period before radical prostatectomy. In one study 30 mg/day of lycopene were given to 15 men in the intervention group while the 11 men were in the control group were instructed to follow the National Cancer Institute's recommendations to consume at least 5 servings of fruits and vegetables daily. Results showed that the lycopene slowed the growth of prostate cancer. Prostate tissue lycopene concentration was 47% higher in the intervention group. Subjects that took the lycopene for 3 weeks had smaller tumors, less involvement of the surgical margins, and less diffuse involvement of the prostate by pre-cancerous high-grade prostatic intraepithelial neoplasia [ 150 ]. In another study before radical prostatectomy surgery 32 men were given a tomato sauce-based pasta dish every day, which supplied 30 mg of lycopene per day. After 3 weeks serum and prostate lycopene levels increaed 2-fold and 2.9-fold, respectively. PSA levels decreased 17%, as seen also by Kucuk et al [ 150 ]. Oxidative DNA damage was 21% lower in subjects' leukocytes and 28% lower in prostate tissue, compared to non-study controls. The apoptotic index was 3-fold higher in the resected prostate tissue, compared to biopsy tissue [ 151 ]. These intervention studies raise the question of what could have been done in this intervention was longer and combined synergistically with other effective intervention methods, such as flax seed, increased selenium and possibly vitamin E, in the context of a diet high in fruits and vegetable?

Vitamin C, or ascorbic acid, has been studied in relation to health and is the most common supplement taken in the USA. Low blood levels of ascorbic acid are detrimental to health (for a recent article see Fletcher et al [ 152 ]) and vitamin C is correlated with overall good health and cancer prevention [ 153 ]. Use of vitamin C for cancer therapy was popularized by Linus Pauling. At high concentrations ascorbate is preferentially toxic to cancer cells. There is some evidence that large doses of vitamin C, either in multiple divided oral doses or intravenously, have beneficial effects in cancer therapy [ 154 - 156 ]. Oral doses, even in multiple divided doses, are not as effective as intravenous administration. Vitamin C at a dose of 1.25 g administered orally produced mean peak plasma concentrations of 135 ± 21 μmol/L compared with 885 ± 201 μmol/L for intravenous administration [ 154 ].

While vitamin C is quite possibly an effective substance, the amounts required for these therapeutic effects are obviously beyond dietary intakes. However, intravenous ascorbate may be a very beneficial adjuvant therapy for cancer with no negative side effects when administered properly.

Other Antioxidants

There are many more substances that will have some benefit for cancer therapy. Most of these substances are found in foods, but their effective doses for therapy are much higher than the normal concentration in the food. For example, grape seed extract contains proanthocyanidin, which shows anticarcinogenic properties (reviewed by Cos et al \ [ 157 ]. Also, green tea contains a flavanol, epigallocatechin-3-gallate (EGCG), which can inhibit metalloproteinases, among several possible other mechanisms [ 158 ]. And there are claims for various other herbal substances and extracts that might be of benefit, which are beyond the scope of this review.

The bacteria that reside in the intestinal tract generally have a symbiotic relationship with their host. Beneficial bacteria produce natural antibiotics to keep pathogenic bugs in check (preventing diarrhea and infections) and produce some B vitamins in the small intestine where they can be utilized. Beneficial bacteria help with food digestion by providing extra enzymes, such as lactase, in the small intestine. Beneficial bacteria help strengthen the immune system right in the gut where much of the interaction between the outside world and the body goes on. Beneficial bacteria can help prevent food allergies. They can help prevent cancer at various stages of development. These good bacteria can improve mineral absorption, maximizing food utilization.

However, the balance of beneficial and potentially pathogenic bacteria in the gut is dependent on the diet. Vegetable fiber encourages the growth of beneficial bacteria. A group of Adventist vegetarians was found to have a higher amount of beneficial bacteria and lower amount of potentially pathogenic bacteria compared to non-vegetarians on a conventional American diet [ 159 ]. Differences in bacterial populations were seen between patients who recently had a colon polyp removed, Japanese-Hawaiians, North American Caucasians, native rural Japanese, and rural native Africans. Lactobacillus species and Eubacterium aerofaciens , both producers of lactic acid, were associated with the populations with the lower risk of colon cancer, while Bacteroides and Bifidobacterium species were associated with higher risk of colon cancer [ 160 ]

There is a solid theoretical basis for why probiotics should help prevent cancer, especially colon cancer, and even reverse cancer. Probiotics produce short chain fatty acids in the colon, which acidify the environment. Lower colon pH is associated with lower incidence of colon cancer. Probiotic bacteria reduce the level of procarcinogenic enzymes such as beta-glucuronidase, nitroreductase, and azoreductase [ 161 ].

L. casei was used in two trials of patients with superficial bladder cancer. In the first trial, the probiotic group had a 50% disease free time of 350 days, compared to 195 days for the control group [ 162 ]. The second trial also showed that the probiotics worked better than the placebo, except for multiple recurring tumors [ 163 ].

Except for the two studies noted above, most of the research of probiotics and cancer has been done in animals. Studies have looked at markers of tumor growth or at animals with chemically induced tumors.

Studies in rats have shown that probiotics can inhibit the formation of aberrant crypt foci, thought to be a pre-cancerous lesion in the colon. Some of the best results were obtained with a probiotic strain consumed with inulin, a type of fructooligosaccharide. Total aberrant crypt foci, chemically induced, were reduced 74% by the treatment of rats with inulin and B. longum , but only 29 and 21% by B. longum and inulin alone, respectively [ 164 ]. There was a synergistic effect in using both products together. Similar synergy was seen in rats with azoxymethane-induced colon cancer in another study. Rats fed Raftilose, a mixture of inulin and oligofructose, or Raftilose with Lactobacilli rhamnosus (LGG) and Bifidobacterium lactis (Bb12) had a significantly lower number of tumors compared to the control group [ 165 ]. A probiotic mixture, without any prebiotic, given to rats fed azoxymethane reduced colon tumors compared to the control (50% vs 90%), and also reduced the number of tumors per tumor-bearing rat [ 166 ].

In lab mice bred to be susceptible to colitis and colon cancer, a probiotic supplement, Lactobacillus salivarium ssp. Salivarius UCC118, reduced fecal coliform levels, the number of potentially pathogenic Clostridium perfringens , and reduced intestinal inflammation. In this small study two mice died of fulminant colitis and 5 mice developed adenocarcinoma in the control group of 10 mice, while there was no colitis and only 1 mouse with adenocarcinoma in the probiotic test group [ 167 ].

The research on probiotics and disease is still an emerging field. There is a high degree of variation of health benefits between different strains of bacteria. As new methods for selecting and screening probiotics become available, the field will be able to advance more rapidly.

Oral Enzymes

Many people diagnosed with cancer have digestion or intestinal tract disorders as well. Impaired digestion will greatly hinder a nutritional approach to treating cancer. If the nutrients cannot be released from the food and taken up by the body, then the excellent food provided by the Hallelujah Diet will go to waste. Digestive enzyme supplements are used to ensure proper and adequate digestion of food. Even raw foods, which contain many digestive enzymes to assist in their digestion, will be more thoroughly digested with less of the body's own resources with the use of digestive enzymes. So, the enzymes taken with meals do not have a direct effect upon a tumor, but assist the body in getting all of the nutrition out of the food for healing and restoring the body to normal function. Recently, an in vitro system was used to test the use of supplemental digestive enzymes. The digestive enzymes improved the digestibility and bioaccessibility of proteins and carbohydrates in the lumen of the small intestine, not only under impaired digestive conditions, but also in healthy human digestion [ 168 ].

There is evidence that indicates the presence of an enteropancreatic circulation of digestive enzymes [ 169 ]. Digestive enzymes appear to be preferentially absorbed into the bloodstream and then reaccumulated by the pancreas for use again. There appears to be a mechanism by which digestive enzymes can reach systemic circulation.

Enzymes, especially proteases, if they reach systemic circulation, can have direct anti-tumor activity. Wald et al [ 170 ] reported on the anti-metastatic effect of enzyme supplements. Mice inoculated with the Lewis lung carcinoma were treated with a proteolytic enzyme supplement, given rectally (to avoid digestion). The primary tumor was cut out, so that the metastatic spread of the cancer could be measured. After surgical removal of the primary tumor (day 0), 90% of the control mice died by day 18 due to metastasized tumors. In the first group, which received the rectal enzyme supplement from the time of the tumor-removal surgery, 30% of the mice had died from metastasized cancer by day 25. In the second group, which received the enzymes from 6 days prior to removal of the primary tumor, only 10% of the animals showed the metastatic process by day 15. In the third group, which received the enzyme treatment since the initial inoculation of the Lewis lung carcinoma, no metastatic spread of the tumor was discernible. One hundred day-survival rates for the control, first, second, and third groups were 0, 60%, 90%, and 100%.

In a similar experiment, an enzyme mixture of papain, trypsin, and chymotrypsin, as used in the preparation Wobe-Mugos E, was rectally given to mice that were inoculated with melanoma cells. Survival time was prolonged in the test group (38 days in the enzyme group compared to 24 days in the control mice) and 3 of the 10 enzyme-supplemented mice were cured. Again, a strong anti-metastatic effect of the proteolytic enzymes was seen [ 171 ].

Further evidence of the efficacy of oral enzyme supplementation is available from clinical trials in Europe. Two different studies have demonstrated that two different oral proteolytic enzyme supplements were able to reduce high levels of transforming growth factor-β, which may be a factor in some cancers [ 172 , 173 ]. In the Slovak Republic an oral enzyme supplement was tested in a placebo-controlled trial of multiple myeloma. For stage III multiple myeloma, control group survival was 47 months, compared to 83 months (a 3 year gain) for patients who took the oral enzymes for more than 6 months [ 174 ].

Enzyme supplements have also been shown to reduce side effects of cancer therapy. Enzyme supplementation resulted in fewer side effects for women undergoing radiation therapy for carcinomas of the uterine cervix [ 175 ], for patients undergoing radiation therapy for head and neck cancers [ 176 ], and for colorectal cancer patients undergoing conventional cancer treatments [ 177 ]. In a large multi-site study in Germany women undergoing conventional cancer therapy were put into a control group or a group that received an oral enzyme supplement. Disease and therapy related symptoms were all reduced, except tumor pain, by the enzyme supplement. Also, survival was longer with less recurrence and less metastases in the enzyme group [ 178 ]. In all of these studies the oral enzyme supplements were well tolerated, with only a small amount of mild to moderate gastrointestinal symptoms.

Even though these few studies don't give a lot of evidence of the effectiveness of oral enzyme supplementation, it is clear that there are some circumstances that will be helped by enzyme supplementation, with very little danger of negative side effects. At the least, enzymes will improve digestion and lessen the digestive burden on the body, leaving more reserves for disease eradication. However, as the research indicates, the effect may be much greater than that, with the potential for direct anti-tumor activity.

Whole Diet Studies

A diet-based cancer therapy, the Gerson Therapy, was used to treat melanoma cancer. The five-year survival rates from their therapy compared very favorably to conventional therapy reported in the medical literature, especially for more advanced stages of melanoma [ 179 ] (see Table ​ Table7 7 ).

Gerson Therapy for Melanoma [179].

An Italian cohort of 8,984 women was followed for an average of 9.5 years, with 207 incident cases of breast cancer during that time. Their diets were analyzed by patterns – salad vegetables (raw vegetables and olive oil), western (potatoes, red meat, eggs and butter), canteen (pasta and tomato sauce), and prudent (cooked vegetables, pulses, and fish). Only the salad vegetable diet pattern was associated with a significantly lower risk of breast cancer, about 35% lower. For women of normal weight (BMI <25) the salad vegetable pattern was even more protective, about a 61% decreased risk of breast cancer [ 180 ]. The overall dietary pattern does make a very significant difference.

In US-based studies the "prudent" diet has been shown to be protective for colon cancer, while the "western" diet has been shown to be detrimental. The "western" dietary pattern, with its higher intakes of red meat and processed meats, sweets and desserts, French fries, and refined grains, was associated with a 46% increase relative risk of colon cancer in the Nurses' Health Study [ 45 ]. Slattery et al [ 17 ] found a two-fold increase in relative risk of colon cancer associated with a "western" dietary pattern, and a 35–40% decrease in relative risk associated with the "prudent" pattern, especially among those diagnosed at an earlier age (<67 years old). The "salad vegetable" pattern is still more likely to be protective compared to the prudent dietary pattern, but this pattern did not exist in this study population.

In an analysis of the colon cancer data from the Health Professionals Follow-up Study, Platz et al [ 56 ] found that there was a 71% decrease in colon cancer risk when men with none of six established risk factors were compared to men with at least one of these risk factors (obesity, physical inactivity, alcohol consumption, early adulthood cigarette smoking, red meat consumption, and low intake of folic acid from supplements). So, if all men had the same health profile as these healthier 3% of the study population, colon cancer rates would have been only 29% of what they measured.

A plant-based dietary pattern in being currently tested in the Women's healthy Eating and Living (WHEL) Study. About 3,000 women who were treated for an early stage of breast cancer have been randomized into two groups. The dietary goals for the test group of the study are 5 servings of vegetables, 16 oz of vegetable juice, 3 servings of fruit, 30 g of fiber, and <20% of energy from fat. No guidelines were given for animal product intake, and initial results seem to confirm, since there were no changes in body weight, total cholesterol, or LDL cholesterol [ 181 ], which would be affected by animal protein intake. However, over the first year of follow-up vegetable intake did increase to seven servings/day, fruit intake increased to 3.9 servings/day, energy from fat decreased from 28% to 23%. Also, plasma carotenoid concentrations increased significantly in the intervention group, but not in the control group. α-Carotene increased 223%, β-carotene increased 87%, lutein increase 29%, and lycopene increased 17% [ 182 ], indicating that a substantial dietary change had been made by these women. It will be very interesting to follow the results of this study.

Conclusions

What is the result when all of these things are put together? What if all of these factors reviewed here were taken into account and put into practice? This anticancer diet would have:

• adequate, but not excessive calories,

• 10 or more servings of vegetables a day, including cruciferous and allium vegetables; vegetable juice could meet part of this goal,

• 4 or more servings of fruits a day,

• high in fiber,

• no refined sugar,

• no refined flour,

• low in total fat, but containing necessary essential fatty acids,

• no red meat,

• a balanced ratio of omega 3 and omega 6 fats and would include DHA,

• flax seed as a source of phytoestrogens,

• supplemented with ~200 μg/day selenium,

• supplemented with 1,000 μg/day methylcobalamin (B-12),

• very rich in folic acid (from dark green vegetables),

• adequate sunshine to get vitamin D, or use 1,000 IU/day supplement,

• very rich in antioxidants and phytochemicals from fruits and vegetables, including α-carotene, β-carotene, β-cryptoxanthin, vitamin C (from foods), vitamin E (from foods),

• very rich in chlorophyll,

• supplemented with beneficial probiotics,

• supplemented with oral enzymes

As reviewed above, reductions of 60 percent in breast cancer rates have already been seen in human diet studies, and a 71 percent reduction in colon cancer for men without the known modifiable risk factors. These reductions are without taking into account many of the other factors considered in this review, such as markedly increased fruit and vegetable intake, balanced omega 3 and 6 fats, vitamin D, reduced sugar intake, probiotics, and enzymes – factors which all are likely to have an impact on cancer. Certainly cancer prevention would be possible, and cancer reversal in some cases is quite likely.

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Immunotherapy is treatment that uses certain parts of a person’s immune system to fight diseases such as cancer. This can be done in a couple of ways:

• Stimulating, or boosting, the natural defenses of your immune system so it works harder or smarter to find and attack cancer cells
• Making substances in a lab that are just like immune system components and using them to help restore or improve how your immune system works to find and attack cancer cells

What the immune system does

Types of cancer immunotherapy.

In the last few decades, immunotherapy has become an important part of treating some types of cancer. New immunotherapy treatments are being tested and approved, and new ways of working with the immune system are being discovered at a very fast pace.

Immunotherapy works better for some types of cancer than for others. It’s used by itself for some of these cancers, but for others it seems to work better when used with other types of treatment.

Your immune system is a collection of organs, special cells, and substances that help protect you from infections and some other diseases. Immune cells and the substances they make travel through your body to protect it from germs that cause infections. They also help protect you from cancer in some ways.

The immune system keeps track of all of the substances normally found in the body. Any new substance that the immune system doesn’t recognize raises an alarm, causing the immune system to attack it. For example, germs contain substances such as certain proteins that are not normally found in the human body. The immune system sees these as “foreign” and attacks them. The immune response can destroy anything containing the foreign substance, such as germs or cancer cells.

The immune system has a tougher time targeting cancer cells, though. This is because cancer starts when normal, healthy cells become changed or altered and start to grow out of control. Because cancer cells actually start in normal cells, the immune system doesn’t always recognize them as foreign.

Clearly there are limits on the immune system’s ability to fight cancer on its own, because many people with healthy immune systems still develop cancer:

• Sometimes the immune system doesn’t see the cancer cells as foreign because the cells aren’t different enough from normal cells.
• Sometimes the immune system recognizes the cancer cells, but the response might not be strong enough to destroy the cancer.
• Cancer cells themselves can also give off substances that keep the immune system from finding and attacking them.

To overcome this, researchers have found ways to help the immune system recognize cancer cells and strengthen its response so that it will destroy them. In this way, your own body is actually getting rid of the cancer, with some help from science.

There are several main types of immunotherapy used to treat cancer, and many are being studied. For more information about immunotherapy as a treatment for a specific cancer, please choose a cancer type .

• Checkpoint inhibitors : These drugs basically take the ‘brakes’ off the immune system, which helps it recognize and attack cancer cells.
• Chimeric antigen receptor (CAR) T-cell therapy : This therapy takes some T-cells from a patient's blood, mixes them with a special virus that makes the T-cells learn how to attach to tumor cells, and then gives the cells back to the patient so they can find, attach to, and kill the cancer.
• C ytokines : This treatment uses cytokines (small proteins that carry messages between cells) to stimulate the immune cells to attack cancer.
• I mmunomodulators : This group of drugs generally boosts parts of the immune system to treat certain types of cancer.
• Cancer vaccines : Vaccines are substances put into the body to start an immune response against certain diseases. We usually think of them as being given to healthy people to help prevent infections. But some vaccines can help prevent or treat cancer.
• Monoclonal antibodies (mA bs or MoA bs): These are man-made versions of immune system proteins. mAbs can be very useful in treating cancer because they can be designed to attack a very specific part of a cancer cell.
• O ncolytic viruses : This treatment uses viruses that have been modified in a lab to infect and kill certain tumor cells.

The American Cancer Society medical and editorial content team

Our team is made up of doctors and oncology certified nurses with deep knowledge of cancer care as well as editors and translators with extensive experience in medical writing.

American Society of Clinical Oncology (ASCO). ASCO Annual Meeting 2019: Immunotherapy for lung cancer, gastrointestinal cancers and targeted therapy for breast cancer . Accessed at cancer.net. Content is no longer available. 

American Society of Clinical Oncology (ASCO). Understanding immunotherapy. Accessed at cancer.net. Content is no longer available. 

Bayer VR, Davis ME, Gordan RA, et al. Immunotherapy. In Olsen MM, LeFebvre KB, Brassil KJ, eds. Chemotherapy and Immunotherapy Guidelines and Recommendations for Practice . Pittsburgh, PA: Oncology Nursing Society; 2019:149-189.

Brodsky AN. Cancer immunotherapy: The year in review and a look at the year ahead . Cancer Research Institute. Accessed at https://www.cancerresearch.org/blog/january-2019/cancer-immunotherapy-2018-review-2019-predict on December 19, 2019.

Coventry BJ. Therapeutic vaccination immunomodulation: Forming the basis of all cancer immunotherapy. Ther Adv Vaccines Immunother. 2019; 1:7:2515135519862234. Accessed at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6676259/ on December 19, 2019.

DeMaria PJ, Bilusic M. Cancer vaccines. Hematol Oncol Clin North Am. 2019; 33(2):199-214.

DeSelm CJ, Tano ZE, Varghese AM, et al. CAR T-cell therapy for pancreatic cancer. J Surg Oncol. 2017; 16(1):63-74.

Gatti-Mays ME, Redman JM, Collins JM, et al. Cancer vaccines: Enhanced immunogenic modulation through therapeutic combinations. Hum Vaccin Immunother . 2017; 13(11):2561-2574. Accessed at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5703410/ on December 19, 2019.

Hafeez U, Gan HK, Scott AM. Monoclonal antibodies as immunomodulatory therapy against cancer and autoimmune diseases. Curr Opin Pharmacol . 2018; 41:114-121.

Hill JA, Giralt S, Torgerson TR, et al. CAR-T- and a side order of IgG, to go?- Immunoglobulin replacement in patients receiving CAR-T cell therapy. Blood Rev. 2019 [Accepted manuscript]. Accessed at https://www.ncbi.nlm.nih.gov/pubmed/31416717 on December 19, 2019.

Ling DC, Bakkenist CJ, Ferris RL et al. Role of immunotherapy in head and neck cancer. Semin Radiat Oncol . 2018; 28(1): 12-16.

Maeng H, Terabe M, Berzofsky JA. Cancer vaccines: Translation from mice to human clinical trials. Curr Opin Immunol . 2018; 51:111-122. Accessed at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5943163/ on December 19, 2019.

Mestermann K, Giavridis T, Weber J, , et al. The tyrosine kinase inhibitor dasatinib acts as a pharmacologic on/off switch for CAR T cells. Sci Transl Med.   [Abstract]. 2019; 11(499).

Myers DR, Wheeler B, Roose JP. mTOR and other effector kinase signals that impact T cell function and activity. Immunol Rev. 2019; 291(1):134-153.

National Cancer Institute (NCI). CAR T cells: Engineering patients’ immune cells to treat their cancers . Accessed at https://www.cancer.gov/about-cancer/treatment/research/car-t-cells on December 19, 2019.

National Cancer Institute (NCI). Immunotherapy to treat cancer . Accessed at https://www.cancer.gov/about-cancer/treatment/types/immunotherapy on December 19, 2019.

Russell SJ, Barber GN. Oncolytic viruses as antigen-agnostic cancer vaccines. Cancer Cell. 2018;33(4): 599-605. Accessed at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5918693/ on December 19, 2019.

Wraith DC. The future of immunotherapy: A 20-year perspective. Front Immunol . 2017:8:1668. Accessed at https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5712390/ on December 19, 2019.

Last Revised: December 27, 2019

American Cancer Society medical information is copyrighted material. For reprint requests, please see our Content Usage Policy .

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Dr Yekedüz on a Case Study of Adjuvant Treatment Options in ccRCC

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Emre Yekedüz, MD, discusses a case study shared via social media that evaluated treatment options for a patient with clear cell renal cell carcinoma.

Emre Yekedüz, MD, research fellow, Dana-Farber Cancer Institute, discusses a case study shared via social media that evaluated treatment options for a patient with clear cell renal cell carcinoma (ccRCC).

In a social media poll to members of the oncology community, which was posted to X (previously Twitter), Yekedüz highlighted a case study that prompted conversations about the applicability of different RCC management avenues.Notably, this was done to raise awareness for World Kidney Cancer Day, which took place on June 20, 2024. The poll read: “[A] 62-year-old man underwent radical nephrectomy for a 75-mm left renal mass diagnosed as ccRCC with sarcomatoid features. [The] tumor invaded perirenal sinus fat but did not [extend] beyond Gerota’s fascia, with clear surgical margins. Imaging revealed no distant metastases. What’s [the] next step?”

The patient in the case was diagnosed with pathological T3 and grade 4 ccRCC with sarcomatoid features, Yekedüz begins. The key question posed by the poll was about the next step for adjuvant treatment for this patient with ccRCC, he reports.

According to the poll results, 69% of responders selected adjuvant pembrolizumab (Keytruda) as the preferred treatment option, Yekedüz explains. This outcome is not unexpected given that the phase 3 KEYNOTE-564 trial (NCT03142334) was the first to demonstrate improved overall survival with pembrolizumab vs placebo in the adjuvant setting in patients with kidney cancer, he says. Prior to these findings, TKIs had not been successful agents for treating patients with early-stage kidney cancer in the adjuvant setting, making the KEYNOTE-564 trial a significant milestone, Yekedüz notes.

The National Comprehensive Cancer Network Guidelines suggest that pembrolizumab should be the first adjuvanttreatment consideration for patients with ccRCC based on KEYNOTE-564 data. However, it’s important to consider individual patient factors, such as preexisting autoimmune diseases, which may increase the risk of immune-related adverse effects during pembrolizumab treatment, he emphasizes. These conditions must be carefully evaluated before initiating therapy, highlighting the importance of personalized treatment approaches in clinical practice, Yekedüz concludes.

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